Then, Chen et al. used Cas9 to disrupt the dystrophin gene (DMD) in rhesus monkeys, which exhibited markedly depleted dystrophin and muscle degeneration seen in early Duchenne muscular dystrophy (DMD) (Chen et al., 2015b), indicating that CRISPR/Cas9 can efficiently generate monkey models of human diseases regardless of inheritance patterns. This evidence concerns the gene DMD and Duchenne muscular dystrophy.